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Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease
Over recent years, several investigations have suggested that Parkinson’s disease (PD) can be regarded as the consequence of a bowel disorder. Indeed, gastrointestinal symptoms can occur at all stages of this neurodegenerative disease and in up to a third of cases, their onset can precede the involv...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7730281/ https://www.ncbi.nlm.nih.gov/pubmed/33276665 http://dx.doi.org/10.3390/ijms21239199 |
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author | Benvenuti, Laura D’Antongiovanni, Vanessa Pellegrini, Carolina Antonioli, Luca Bernardini, Nunzia Blandizzi, Corrado Fornai, Matteo |
author_facet | Benvenuti, Laura D’Antongiovanni, Vanessa Pellegrini, Carolina Antonioli, Luca Bernardini, Nunzia Blandizzi, Corrado Fornai, Matteo |
author_sort | Benvenuti, Laura |
collection | PubMed |
description | Over recent years, several investigations have suggested that Parkinson’s disease (PD) can be regarded as the consequence of a bowel disorder. Indeed, gastrointestinal symptoms can occur at all stages of this neurodegenerative disease and in up to a third of cases, their onset can precede the involvement of the central nervous system. Recent data suggest that enteric glial cells (EGCs) may play a major role in PD-related gastrointestinal disturbances, as well as in the development and progression of the central disease. In addition to their trophic and structural functions, EGCs are crucial for the homeostatic control of a wide range of gastrointestinal activities. The main purpose of this review was to provide a detailed overview of the role of EGCs in intestinal PD-associated alterations, with particular regard for their participation in digestive and central inflammation as well as the dynamic interactions between glial cells and intestinal epithelial barrier. Accumulating evidence suggests that several pathological intestinal conditions, associated with an impairment of barrier permeability, may trigger dysfunctions of EGCs and their shift towards a proinflammatory phenotype. The reactive gliosis is likely responsible for PD-related neuroinflammation and the associated pathological changes in the ENS. Thus, ameliorating the efficiency of mucosal barrier, as well as avoiding IEB disruption and the related reactive gliosis, might theoretically prevent the onset of PD or, at least, counteract its progression. |
format | Online Article Text |
id | pubmed-7730281 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-77302812020-12-12 Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease Benvenuti, Laura D’Antongiovanni, Vanessa Pellegrini, Carolina Antonioli, Luca Bernardini, Nunzia Blandizzi, Corrado Fornai, Matteo Int J Mol Sci Review Over recent years, several investigations have suggested that Parkinson’s disease (PD) can be regarded as the consequence of a bowel disorder. Indeed, gastrointestinal symptoms can occur at all stages of this neurodegenerative disease and in up to a third of cases, their onset can precede the involvement of the central nervous system. Recent data suggest that enteric glial cells (EGCs) may play a major role in PD-related gastrointestinal disturbances, as well as in the development and progression of the central disease. In addition to their trophic and structural functions, EGCs are crucial for the homeostatic control of a wide range of gastrointestinal activities. The main purpose of this review was to provide a detailed overview of the role of EGCs in intestinal PD-associated alterations, with particular regard for their participation in digestive and central inflammation as well as the dynamic interactions between glial cells and intestinal epithelial barrier. Accumulating evidence suggests that several pathological intestinal conditions, associated with an impairment of barrier permeability, may trigger dysfunctions of EGCs and their shift towards a proinflammatory phenotype. The reactive gliosis is likely responsible for PD-related neuroinflammation and the associated pathological changes in the ENS. Thus, ameliorating the efficiency of mucosal barrier, as well as avoiding IEB disruption and the related reactive gliosis, might theoretically prevent the onset of PD or, at least, counteract its progression. MDPI 2020-12-02 /pmc/articles/PMC7730281/ /pubmed/33276665 http://dx.doi.org/10.3390/ijms21239199 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Benvenuti, Laura D’Antongiovanni, Vanessa Pellegrini, Carolina Antonioli, Luca Bernardini, Nunzia Blandizzi, Corrado Fornai, Matteo Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease |
title | Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease |
title_full | Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease |
title_fullStr | Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease |
title_full_unstemmed | Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease |
title_short | Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease |
title_sort | enteric glia at the crossroads between intestinal immune system and epithelial barrier: implications for parkinson disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7730281/ https://www.ncbi.nlm.nih.gov/pubmed/33276665 http://dx.doi.org/10.3390/ijms21239199 |
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